The long-term goal of these studies is to understand how sensory information about the environment is transformed into motor commands that guide adaptive behavior. In this context, the neural mechanisms underlying the control of vocalization in response to auditory feedback in the mammalian central nervous system will be investigated. Focus is on the significance of certain neurons (VOC-inhibition neurons) situated in the midbrain paralemniscal tegmentum for auditory feedback control of vocalizations in awake, behaving horseshoe bats. These bats accurately control the frequency of their echolocation calls through auditory feedback both when the bat is at rest (resting frequency) and when it is flying and compensating for frequency-shifted echo signals (Doppler-shift compensation behavior). Previous studies suggest that VOC-inhibition neurons in the paralemniscal tegmentum play an important role in the control of vocalization frequencies through an inhibitory auditory feedback mechanism. This hypothesis will be verified by employing an experimental approach that proved to be successful in previous studies on the sensory-motor control of another vertebrate behavior, the "Jamming Avoidance Response" in electric fish. Specifically: (1) It will be tested whether paralemniscal VOC-inhibition neurons are actively involved in the control of the resting frequency and of Doppler-shift compensation behavior. For that purpose, the region containing these neurons will be identified stereotaxically and electrophysiologically and then VOC- inhibition neurons will be reversibly inactivated with the GABA agonists Muscimol (GABA-A, R(+)Baclofen (GABA-B), and trans-4-aminocrotonic acid (GABAC), respectively, while the resting frequency and the Doppler-shift compensation behavior are monitored. (2) It will be determined whether VOC-inhibition neurons provide auditory feedback by means of an inhibitory or excitatory mechanism. This will be achieved by stimulating VOC- inhibition neurons with the Glutamate agonists NMDA, AMPA, and Kainic acid, respectively, while monitoring the effects of glutamate agonist injections on the vocalization frequency. If audio-vocal feedback is inhibitory, stimulation and thus increasing neuronal activity should decrease vocalization frequencies emitted at rest and during Doppler-shift compensation while they should increase if the feedback is excitatory. The results of these studies will provide new insights into the neural implementation of audio-vocal control mechanisms in awake, behaving animals and could also provide an approach to better understand various malfunctions of basic parameters of human voice, such as changes in the fundamental frequency that occur in speaking deaf humans.